Research Paper Volume 13, Issue 9 pp 12929—12954
Prognostic and immunological potential of PPM1G in hepatocellular carcinoma
- 1 Department of Oncology, Shunyi Hospital of Beijing Traditional Chinese Medicine Hospital, Beijing, China
- 2 Department of Oncology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Dongcheng, Beijing, China
Received: September 25, 2020 Accepted: April 2, 2021 Published: May 5, 2021https://doi.org/10.18632/aging.202964
How to Cite
Copyright: © 2021 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Liver hepatocellular carcinoma (LIHC) remains one of the most common causes of cancer death. Prior research suggested that the PPM1G gene is involved in LIHC. To explore the role of PPM1G in LIHC, we used several online databases. Expression profiling was performed via the Gene Expression Profiling Interactive Analysis (GEPIA), Hepatocellular Carcinoma Database (HCCDB), Oncomine and Human Protein Atlas (HPA) platforms. Mutation profiles were investigated via cBio Cancer Genomics Portal (cBioPortal). Survival analysis was performed via the Kaplan–Meier (KM) plotter and International Cancer Genome Consortium (ICGC) platforms. The biological function of PPM1G was analyzed via the Enrichr database. The influence of PPM1G expression in the tumor immune microenvironment was assessed via Tumor Immune Estimation Resource (TIMER). PPM1G expression was upregulated in various tumors, including LIHC. Overexpression of PPM1G was associated with poor prognosis in LIHC. PPM1G expression might be regulated by promoter methylation, copy number variations (CNVs) and kinases and correlate with immune infiltration. The gene ontology (GO) terms associated with high PPM1G expression were mRNA splicing and the cell cycle. The results suggest that PPM1G is correlated with the prognosis of LIHC patients and associated with the tumor immune microenvironment in LIHC.
LIHC: liver hepatocellular carcinoma; GEPIA: Gene Expression Profiling Interactive Analysis; HCCDB: Hepatocellular Carcinoma Database; HPA: Human Protein Atlas; cBioportal: cBio Cancer Genomics Portal; KM: Kaplan–Meier; ICGC: International Cancer Genome Consortium; CNVs: copy number various; TIMER: Tumor Immune Estimation Resource; GO: genetic oncology; PPM: metal-dependent protein phosphatase; PP2C: protein phosphatase 2C; ESCC: esophageal squamous cell carcinoma; GENT: Gene Expression across Normal and Tumor Tissue; TCGA: The Cancer Genome Atlas; GEO: Gene Expression Omnibus; TCGA -LIHC: Liver Hepatocellular Carcinoma Project of The Cancer Genome Atlas; ICGC-LIRI-JP: Liver Cancer-RIKEN, JP Project from International Cancer Genome Consortium; AMP: amplification; OS: overall survival; DFS: disease free survival; PFS: progression free survival; RFS: recurrence-free survival; DSS: disease-specific survival; TISIDB: Tumor-Immune System Interactions Database; UCSC: University of California Santa Cruz; KEGG: Kyoto Encyclopedia of Genes and Genomes; TF: transcription factor; PPI: protein-protein interaction; CNAs: Copy Number Alterations; GISTIC: genomic identification of significant targets in cancer; GSEA: gene set enrichment analysis.